Raina shares her thoughts on how to get the most out of your thyroid medication.

Since my diagnosis in 2012, I have been on a journey to comprehend the complexities of thyroid disease. I admit I knew very little prior to my actual diagnosis. My health focus was on cardiovascular disease and diabetes, as these were actually preventable health issues. Once diagnosed with Hashimoto’s, I began to understand how some things are just out of your control and no matter how healthy you are one turn of a chemical switch can alter everything you have even known.

Understanding, that I actually had two different conditions, my journey became about researching the one condition Doctors did not have an answer for, the autoimmune disease Hashimoto’s. The varying symptoms of this disease can be different for each person in intensity and severity. What causes these symptoms and what could be done to lessen them or eliminate them all together? I have been researching this for just over 3 years…and this is my conclusion; We change our diets, our lifestyles and our bad habits…all of which we will benefit from, but none of these things will do the one thing that can help us function better. The autoimmune disease is just one part of the puzzle and we cannot forget about what the actual disease causes, hypothyroid.

Until most recently, my personal focus has been reducing the symptoms of Hashimoto’s, but once I accomplished this for myself…I still felt I needed more. Inflammation is the key to every disease known to man and reducing this in your body is good for prevention and management for any disease that you may have. This is especially true in autoimmune diseases, as well as diabetes and heart disease. When it comes to the thyroid gland itself, I was leaving this up to my doctor since the only answer was the thyroid hormone replacement. Get tested, if your numbers are off, get adjusted….simple, NOT. I have spent the last 9 months working on getting my antibodies down and eliminating the autoimmune symptoms…the last month. I have been researching why we have a hard time getting in optimal range with our thyroid medication’s and staying there. Why do we need this constant adjusting up & down? Why do some need T3 and some do not? Why do some do well with amour and why some do not? We all know we are chemically different and that is accepted in the community, but is there a solution to these questions? Once we get the autoimmune disease calmed, how do we get the most out of medicine?

I am a firm believer in less is more; less stress, more benefits. Taking more medicine is more stressful on the organs in the body, taking more supplements is, as well. If I could find a way not to need more medicine of any-kind to feel better, the better my liver would be.

The liver is the main organ responsible for filtering everything we consume, breath in and apply to our skin. Keeping this organ in good working condition is imperative for health. The liver is also where our cholesterol and hormones are produced, digestion, and detoxification takes place, and protein synthesis as well as, our metabolism are all part of liver function. All medications and supplements must be filtered through the liver and therefore a constant evaluation of what we are doing must be part of our healing journey.

A look at the thyroid and it’s relation to the organs in the body

Thyroid cells are the only cells in the body which can absorb iodine. These cells combine iodine and the amino acid tyrosine to make T3 and T4. T3 and T4 are then released into the blood stream and are transported throughout the body where they control metabolism (conversion of oxygen and calories to energy).

This process is called 5’deiodinase and this occurs in 3 specific types (D1, D2 and D3) each of these happen within a different set of organs within the body. The deiodination is the removal of one iodine molecule from T4 to produce T3 and then further conversion to T2.

1) 3,5-Diiodothyronine (T2) is on a role. A new hormone in search of recognition.

Most of the deiodination takes place within the liver and a lesser degree in the kidneys and skeletal muscles of type 1 (D1).

Type 1(D1), is the process of converting T4 to T3, as well as T4 to reverse T3. This takes place within the liver, kidneys and skeletal muscle. Approximately 60% of T4 is converted to T3 and 40% to rT3. This is where the ratio calculation comes into play. When you have reverse T3 tested, the test result means very little without a test result of T3 and or FreeT3. Reverse T3 gets divided into T3 or Ft3 and your result is a ratio of the actual conversion. A given number higher than 20 is a good conversion ratio of T4 to T3 and less than 20 is a higher conversion ratio of T4 to rT3.

Type 2( D2) , is the process of converting T4 to T3 only and this takes place in the brain, pituitary gland and brown adipose tissue. There is no T4 to rT3 conversion in D2. What can occur is a defunct or defect of the bodies ability to convert within the (D2) Deiodinase, which leads to the possible conversion to Type 3 deiodinase.

Type 3(D3), is the process of converting T4 to reverse T3 only and this takes place with in the central nervous system.

Clearance of reverse T3 is an activity that occurs within the body systems, this helps prevent the excess buildup of reverse T3 within our organs. Anti-oxidant enzymes are responsible for this action and may actually shed some light as to why some thyroid patients are more symptomatic than others. Remember, we all convert some percentage of T4 to reverse T3, how much and how much builds up, may be something we can control.

Antioxidant Enzyme Systems and Lipid Peroxidation

The roles of lipid peroxidation and antioxidant enzyme systems have also received some attention with respect to thyroid hormone metabolism. There is a relationship between hepatic lipid peroxidation and peripheral conversion of T4 to T3 has been observed in animal experiments. This knowledge has led some researchers to speculate that alterations in antioxidant status may influence how well the thyroid functions and how it affects metabolism. The liver has an important role in thyroid hormone metabolism; it is very possible this might be compromised if the liver is subjected to chemicals/toxins and the inability to clear out rT3.

The connection between hepatic (liver) antioxidant enzyme system activity, lipid peroxidation, and peripheral conversion of T4 to T3 in animal models after administration of specific botanical extracts, minerals and vitamins more than suggest a possible interaction between this aspect of liver function and thyroid hormone metabolism. Since there are differences between animals and humans, the actions of these metabolic pathways to thyroid hormone metabolism is not clear and have not been fully studied in humans.

We know the factors that can interfere with proper conversion, absorption and clearance; Stress, other drugs, lack of sleep, high or low cortisol levels, caloric restriction, carbohydrate restriction, too much exercise and intensity of exercise, lifestyle and other illnesses or diseases.

When it comes to the liver and its function, there is one thing that can severely affect proper function and that is alcohol consumption.

Alcohol Intake was tested in animal models and was shown to impair hepatic 5′-deiodination. Patients with alcohol-induced liver cirrhosis, low T3 and T4, elevated rT3, and normal TSH values have been observed. In these subjects an abolished circadian rhythm causing sleep deprivation issues and elevated cortisol levels have frequently been observed. While extreme alcohol-induced liver damage is apparently detrimental to the peripheral conversion of thyroid hormones, it is only an assumption that moderate consumption of alcohol would have the same affect. Based on my personal experience, I have noticed a difference in energy, over-all mood and sensation of wellness after drinking 1-2 cocktails. When abstaining for alcohol consumption, I have noticed a considerable difference in how I feel in regards to daily activities and overall mood. Since the liver is primarily where deiodinase and conversion occurs, it makes sense to focus on the health and status of liver function.

There are many foods, herbs, nutrients and botanicals that can affect thyroid function both positively and/or negatively, choosing these wisely will be most important when trying to achieve the most out of your thyroid medication and dosage. For simplicity purposes, I have only included the ones that have been proven to significantly enhance the deiodinase process (conversion of T4 to T3 to T2), as well as the clearance of rT3 out of the body tissues.

Selenium

Selenium, as selenocysteine, is a cofactor for type I hepatic 5′-deiodinase, this trace mineral has received the most attention with respect to peripheral metabolism of thyroid hormones. Selenium deficiency apparently decreases or impairs the deiodinase activity. The result would be a decrease in efficiency or ability to deiodinate T4 to T3 and lead to a decreased ability to degrade and clear RT3 out of body tissues. This trace mineral has the ability to assist in the conversion of T4 to T3 and then on to T2 within the Type 1 deiodinase (liver, kidneys and skeletal muscle).

Zinc

Selenium is a co-factor of 5’deiodinase, which means it effects the conversion process within the organs itself… but Zinc is not a co-factor and its part in thyroid hormone metabolism does not directly occur within the organ but within the blood instead. Zinc assists with further conversion of T3 to T2. Therefore, a deficiency in zinc has no effect on T4 hormones, but does decrease levels in T3 and fT4 by 30%. A notable reduction by 67% in Type 1 deiodinase, suggests it also assists in part in the liver, but not as a co –factor.

This means that if you test low in zinc, this alone could be effecting that actual conversion of T4 to T3 with in the liver, kidneys and skeletal muscle. Including a small dose of zinc in your regime may help with making the most of your thyroid hormone medicine.

Flavonoids

Unfortunately, these natural and synthetic antioxidants are the most active INHIBITOR of the 5’ deiodinase conversion process of thyroid hormone metabolism. Luteolin, has the most significant negative effect on this activity, other flavonoid structures like; Quercetin, acerola and many other flavonoids also having this inhibitory effect. Soy falls into this group and so does all water soluble vitamin C, as they usually contain the flavonoids mentioned above. Soy has been shown to create a thyroid profile similar to euthyroid sick syndrome, low T3 and diets high in isoflavonoids 128mg/per day has been reported to decrease Free T3. Soybeans consumed daily by 37 healthy adults for 1-3 months increased TSH levels, the levels remained within range. Their symptoms included; slower metabolic rate, sleepiness, constipation, as well as goiters and symptoms returned to normal after elimination soybeans of their diet for a month. Niacin, which is being used in the treatment for high cholesterol, significantly decreases serum T4 and T3. There were no changes in TSH and fT4, once again the discontinuation of intake of Niacin resulted in a return to normal levels.

Searching high and low for a vitamin C that did not include any flavonoids was impossible. The only source I was able to find was a fat soluble source of Vitamin C (Ascorbyl Palmitate). Since fruit contain this antioxidant naturally, eliminating them out of your diet should make sense. I am not suggesting that anyone remove fruit form their diet. What I am saying is that taking supplements that contain flavonoids, especially with our thyroid medicine may help with absorption, but decrease the 5’deiodinase process and clearance of rt3. Those of you taking vitamin C along with the thyroid medication may want to discontinue doing so or change to a fat soluble form of vitamin C. Note that all fat soluble vitamins should be taken in the lowest form possible (250-500mg) would be best.

Vitamin E

Combining both vitamin E & vitamin C, has shown to partially restore normal thyroid function and detox the body of heavy metal toxins. Vitamin E at a dose of 5mg/ per body weight on alternating days, Improved significantly the 5’deiodinase activity and heavy metal toxins that leads decreases in T3 within the liver. Taking vitamin E along with curcumin decreases inflammation in the body, so this combination is a powerful tool for autoimmune diseases as well. Again a low dose of vitamin E is suggested {100mg -200mg}.

B-12 vitamins

Animal studies have indicated that deficiency of B12 would result in a slight decrease in Type 1 deiodinase activity within the liver and a significant decrease in T3 within the blood. Those who have issues absorbing B vitamins may want to consider find a B-12 intrinsic factor for better absorption. This also would be best in a smaller dose.

Dandelion Root

Dandelion root (Taxaxacum Officinale) has Antioxidant enzymes that effect lipid peroxidation, a factor in clearance in rT3 from the body tissues. This is the only botanical besides Vitamin C & E that do both, increase Type 1 -5’deiodinase and the enzyme activity that clears the buildup of rT3.

For inflammation reduction for autoimmune disease

Black seed cumin oil has been shown to help with an increase of 5-HT and help alleviate depressive states. It also has anti-cancer activity, anti-inflammatory properties for autoimmune disease and directly effects cognitive abilities.

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1 comment

I am taking Cytomel. Do I need to do all this supplimentation since I only take a T3 already? If not, why doesn’t everyone just go straight to taking a T3 medication and skip all the drama of bodily conversion? There must be a reason I’m not aware of. Also, should I be taking a medication with T4 and T3? I don’t fully understand this aspect of treatment. Thank you for your insight.